Ascites: Diagnosis and Management: Clinical Medicine
Ascites: Diagnosis and Management: Clinical Medicine
Ascites: Diagnosis and Management: Clinical Medicine
Abstract
Ascites, the collection of fluid in the peritoneal cavity, occurs with a variety of disease states. It is one of the earliest and most
common complication of chronic liver disease. In cirrhosis, it is associated with circulatory dysfunction characterized by
arterial vasodilatation, high cardiac output and stimulation of vasoactive systems.
As appropriate treatment depends on accurate diagnosis, paracentesis should be performed in every patient with new onset
ascites to determine the cause and to detect potential complications. The treatment of ascites due to causes other than
chronic liver disease is based on the underlying disease. In ascites associated with chronic liver disease, a combination of low
sodium diet and the administration of diuretics remains the mainstay of therapy. Large volume paracentesis along with
infusion of albumin is the preferred treatment for refractory ascites. The recently introduced technique of transjugular
intrahepatic portosystemic shunt for the management of refractory ascites needs further evaluation.
Introduction Malignancies
Peritoneal carcinomatosis
In clinical practice, the term ‘ascites’ refers to the Lymphomas and leukaemias
detectable and pathologic collection of fluid in the Primary mesothelioma
peritoneal cavity. Usually it is a clinical finding and Miscellaneous
can be confirmed by a diagnostic paracentesis. Chylous ascites
Subclinical amount of fluid (i.e., less than 1.5 litre) Systemic lupus erythematosus
can be detected using ultrasonography or computed Ovarian disease
tomography of the abdomen. Pancreatic ascites
Pseudomyxoma peritonei
Aetiology
Chronic liver disease with portal hypertension,
Pathogenesis
congestive cardiac failure, tuberculosis and In a large number of patients, cirrhosis of liver is the
malignancy are important causes of ascites. However, cause of ascites. Several factors contribute to the
it can occur secondary to a number of pathological development of ascites in chronic liver disease. Kidney
conditions. Various causes of ascites are shown in plays a central role and is responsible for sodium
Table I1 and water retention, through complex mechanisms.
Table I : Causes of Ascites The mechanism by which the diseased liver affects
renal function is not fully understood. The ‘peripheral
Venous hypertension arterial vasodilatation hypothesis’ proposed in 1988
Cirrhosis of liver is based on the presence of characteristic circulatory
Congestive cardiac failure
abnormalities seen in cirrhotic patients 2. These
Constrictive pericarditis
patients show manifestations of increased cardiac
Hepatic venous outflow obstruction
Acute portal vein thrombosis
output, arterial hypotension, decreased peripheral
vascular resistance and splanchnic vasodilatation.
Hypoalbuminemia
Possible causes for vasodilatation include
Cirrhosis of liver
portosystemic shunting and/or impaired clearance of
Nephrotic syndrome
Malnutrition
vasodilator substances like nitric oxide, endotoxins,
prostacyclin, glucagon and adenosine. This peripheral
Infections and splanchnic vasodilatation is perceived as
Tuberculosis
reduction in effective plasma volume. The effective
Parasitic (strongyloidosis, entamoeba)
hypovolumia brings into play the baroreceptor
* Additional Professor, Department of Medicine mediated activation of renin - angiotensin -
All India Institute of Medical Sciences, aldosterone system and sympathetic nervous system
New Delhi-110 029 which produce renal vasoconstriction and salt and
water retention (Fig. 1)2,3. • decreased oncotic pressure of plasma due to
impaired albumin production by the liver;
Cirrhosis • portal hypertension which localizes the fluid within
t the peritoneal cavity; and
t t
Portal hypertension Deranged liver function • an increased production of hepatic lymph due to
post-sinusoidal obstruction by the hepatic
t nodules1.
Portal-systemic shunt
In ascites associated with other conditions, the
t t pathogenesis depends on the cause. In congestive
Accumulation of vasodilator substances cardiac failure, elevation of right sided cardiac
(NO, Prostacyclin, Adenosine, Endotoxins) pressures results in the congestion of hepatic sinusoids
Cytokines and leakage of fluid from the surface of liver. In
addition, reduction in effective blood volume leads
t to sodium and water retention by the kidney4. In
Peripheral and splanchnic vasodilatation
ascites associated with non-hepatic malignant
t
disease, the pathogenesis depends on the type and
Effective hypovolumia location of tumour5. In peritoneal carcinomatosis, the
most common cause of malignant ascites, the leakage
t of protein rich fluid from the malignant cells causes
Renin - angiotensin - aldosterone system exudation of extracellular fluid into the peritoneal
Antidiuretic hormone secretion cavity. Large liver tumours pressing on or growing
Sympathetic nervous activity
into the portal or hepatic veins can cause portal
t hypertension and ascites. Infiltration of lymphatic
t t
Renal Sodium and channels by malignant disease especially lymphoma
vasoconstriction water retention may lead to rupture of lymphatics and thereby
t produce chylous ascites. Chylous ascites can also
t t occur after transection of lymphatics, such as after
Increased Impaired t abdominal surgery6. Filarasis is another uncommon
renal renal Ascites formation but important cause of chylous ascites.
prostaglandin prostaglandin
synthesis synthesis Pancreatic ascites results from rupture of the
(e.g. due to drugs) pancreatic duct or leakage of the pancreatic secretions
from a pseudocyst. Irritation of the peritoneum by
t the pancreatic secretions can cause accumulation of
Preservation of t protein rich exudate in the peritoneal cavity. Biliary
renal Renal failure
ascites forms by similar mechanism. In infections such
haemodynamics
as tuberculosis, the mechanism is similar to that in
Figure 1 : Factors involved in initiation and maintenance of sodium retention carcinomatosis. There is leakage of protein rich fluid
and renal dysfunction in patients with cirrhosis.
into the peritoneal cavity by the inflamed peritoneum.
The mechanism of ascites in nephrotic syndrome and
In patients with ascites, renal secretion of
dialysis associated ascites is unclear but is probably
prostaglandins, particularly PGE 2 may help to
related to volume expansion and abnormal peritoneal
preserve renal function by maintaining glomerular
permeability. Hypoalbuminaemia also contributes to
filtration and free water clearance. When this renal
ascites in nephrotic syndrome.
PGE2 production falls, perhaps due to renal deficiency
of the precursor arachidonic acid, renal function
deteriorates. Drugs which inhibit prostaglandin Diagnosis
synthetase e.g., NSAIDs may lead to deterioration of
History
renal function and should be avoided in these
patients. Other factors that contribute to ascites Ascitic fluid may accumulate rapidly or gradually
formation in cirrhosis are: depending upon the cause. Mild ascites may not